Hypoxemia alone does not explain blood pressure elevations after obstructive apneas

Ringler, J.; Basner, Robert C.; Shannon, Richard P.; Schwartzstein, Richard M.; Manning, Harold L.; Weinberger, Steven E.; Weiss, J. Woodrow

doi:10.1152/jappl.1990.69.6.2143

Cited by 203 publications

(113 citation statements)

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“…In general, cardiovascular variables fluctuate during the apnea-interapnea periods because of mechanical alterations and reflex changes in autonomic tone. Reflex effects leading to changes in autonomic tone may be activated through 1) changes in thoracic mechanics from obstructed respiratory efforts (4), 2) changes in blood-gas tensions (hypoxia and/or hypercapnia) (12,18), and 3) postapneic arousals. These factors ultimately culminate in an increase in sympathoadrenal tone (9,13), which is associated with a pressor response during the apnea and postapnea periods.…”

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“…Our data demonstrate that the pressor response to apneas in this model is dependent to a large extent on the vagus nerve. Sympathetic activation during periodic apneas is thought to occur from reflex effects elicited from hypoxia, possibly hypercapnia and mechanical alterations (6,9,12,13,18). These physiological alterations cause activation of peripheral and central sensors, including baroreceptors, chemoreceptors, and mechanoreceptors.…”

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Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

Slamowitz

Chen

Scharf

1999

Journal of Applied Physiology

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Slamowitz, D., L. Chen, and S. M. Scharf. Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs. J. Appl. Physiol. 86(6): 1890-1896, 1999There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; ϩ19 Ϯ 25%, P Ͻ 0.05), systemic vascular resistance (SVR; ϩ33 Ϯ 16%, P Ͻ 0.0005), and heart rate (HR; ϩ5 Ϯ 6%, P Ͻ 0.05) and decreased cardiac output (CO) and stroke volume (SV; Ϫ16 Ϯ 10% P Ͻ 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (ϳ14%, P Ͻ 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes. apnea; vagus; hemodynamics OBSTRUCTIVE SLEEP APNEA is a relatively common clinical condition in which upper airway collapse and cessation of airflow produce an acute cardiovascular response, including elevations in blood pressure as well as changes in heart rate and ventricular function (3,24,26). In general, cardiovascular variables fluctuate during the apnea-interapnea periods because of mechanical alterations and reflex changes in autonomic tone. Reflex effects leading to changes in autonomic tone may be activated through 1) changes in thoracic mechanics from obstructed respiratory efforts (4), 2) changes in blood-gas tensions (hypoxia and/or hypercapnia) (12, 18), and 3) postapneic arousals. These factors ultimately culminate in an increase in sympathoadrenal tone (9, 13), which is associated with a pressor response during the apnea and postapnea periods. Studies to date have focused mainly on the relative effect of these physiological alterations with regard to the overall cardiovascular response to apneas. However, few studies have examined specific autonomic pathways mediating this response. In particular, little is known about the relative contribution of vagal traffic in the modulation of the sympathetic response. The vagus nerve could play a prominent role in the cardiovascular response to apneas because of afferent and/or efferent autonomic signals carried within the nerve. Sensory afferent signals from aortic receptors (baroreceptors and/or chemoreceptors) or mechanoreceptors carried via the vagus could be responsible for the augmentation in sympathetic tone during apneas (1, 25). In addition, mechanoreceptor afferents carried via the vagus could increase sympathetically mediated responses through an arousal mechanism (11,14)....

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Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

Slamowitz

Chen

Scharf

1999

Journal of Applied Physiology

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“…Não se sabe exatamente por que a PA dos pacientes com SASO se eleva durante o sono, alguns estudos assinalam que não é devido à hipoxemia (11) , mas sim devido à fragmentação do sono, isto é, a PA se eleva quando ocorre o microdespertar (12) , mas este é um assunto controvertido (13) .…”

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Medicina do sono

Viegas

Tavares

1999

J. Pneumologia

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No último encontro da American Thoracic Society, em abril de 1999, realizado em San Diego, CA, foram apresentados três trabalhos de autores brasileiros sobre medicina do sono, que passamos a comentar.O primeiro deles, feito em parceria entre a PUCRS (Porto Alegre) e a Universidade de Toronto (Canadá), estuda qualitativamente o óxido nítrico (NO) nasal e exalado, em pacientes portadores de síndrome da apnéia do sono obstrutiva (SASO). Os autores não encontram diferença estatisticamente significativa quando comparam os níveis de NO dos pacientes com SASO e indivíduos normais. Então, especulam que ou o NO não reflete o tipo de inflamação encontrada na SASO, ou existiram fatores de confusão no estudo que modificaram os níveis do NO. Considerando que existe inflamação na SASO e que o NO é um marcador inespecífico de inflamação (1) e regulador do tônus broncomotor (2) , optamos pela possibilidade de fatores de confusão no referido estudo, uma vez que outros autores (3) encontraram níveis elevados de NO em pacientes portadores de SASO após o sono, quando comparados com níveis dos mesmos pacientes antes do sono, bem como com valores antes e após o sono de indivíduos normais. Portanto, nos parece razoável concluir que os ní-veis de NO encontram-se elevados em pacientes portadores de SASO apenas após o sono, momento em que a inflamação das vias aéreas superiores se encontra manifesta.O segundo trabalho, realizado em parceria com o Hôpital Saint-Antoine, Paris, e a Universidade Federal do Espírito Santo, diz respeito ao surgimento de hipertensão arterial (HA) no pós-operatório de pacientes normotensos submetidos à uvupalatofaringoplastia. Um dos assuntos em medicina que mais vem ensejando pesquisas clínicas e experimentais é o da associação entre síndrome de apnéia do sono obstrutiva e a hipertensão arterial. Aproximadamente 50% dos pacientes com SASO grave têm HA (4,5) e cerca de 30% dos pacientes com hipertensão arterial essencial têm SASO (6,7) . Por outro lado, pacientes com HA e SASO tratados com continuous positive airway pressure (CPAP) melhoram a HA (8,9) . Entretanto, mesmo havendo uma evidente relação entre a SASO e a HA, alguns autores têm negado esta associação, preferindo atribuí-la à idade, obesidade, ingestão de álcool, etc., que freqüentemente acompanham tanto uma como outra condição (10) .À HA que se manifesta em sono nos portadores de SASO chamamos hipertensão arterial aguda noturna e aparentemente nada tem a ver com a HA crônica diurna, que também ocorre nesses pacientes. Não se sabe exatamente por que a PA dos pacientes com SASO se eleva durante o sono, alguns estudos assinalam que não é devido à hipoxemia (11) , mas sim devido à fragmentação do sono, isto é, a PA se eleva quando ocorre o microdespertar (12) , mas este é um assunto controvertido (13) .A associação entre HA e uvopalatofaringoplastia, conforme descrita no resumo em pauta, é pouco conhecida na literatura. A hipótese levantada pelo autor, de que seria conseqüente à estimulação simpática, parece ser a melhor. Segundo o resumo, os pacientes t...

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“…A similar cardiovascular response is also associated with central apneas in children with SDB (14). In addition, respiratory events may be associated with hypoxia and arousal, both of which have cardiovascular sequelae, increasing BP, HR, and sympathetic activity (15)(16)(17)(18). It is thought that the cardiovascular morbidity associated with SDB may in part be a consequence of the repetitive swings in BP and HR associated with respiratory events (for review see ref.…”

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Augmented cardiovascular responses to episodes of repetitive compared with isolated respiratory events in preschool children with sleep-disordered breathing

et al. 2015

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Data presented as mean ± SEM or median (range). *P < 0.05; † P < 0.001. HR, heart rate; PTT, pulse transit time. Articles Walter et al. Cardiovascular Consequences of Repetitive vs. Isolated Respiratory EventsFor the episodes of repetitive events, the % change in HR from late to between events and from late event to postepisode were significantly higher when compared with the % change in HR from late to postevent in isolated respiratory events (P < 0.001 for both), as shown in Figure 2a. The % change in PTT from late event to postepisode was significantly greater (indicating a greater change in BP) for repetitive episodes when compared with the % change from late to postevents in isolated respiratory events (P < 0.05) (Figure 2b). There was no difference between % change in PTT from late to between events in repetitive episodes compared with % change from late to postevents in isolated respiratory events. The ratio of repetitive to isolated respiratory events for each child significantly predicted the mean HR, which increased with an increasing proportion of repetitive respiratory events compared with isolated events during N1, N2, REM, and total sleep (Figure 3). There were no relationships between mean PTT and the ratio of repetitive to isolated respiratory events during wake or any sleep stage. Determinants of Percentage Change in HR and PTT From Lateto Between-Event Phases in Episodes of Repetitive Respiratory EventsResults of the multiple linear regression analysis indicate that during total sleep, the repetitive to isolated events ratio, the number of individual respiratory events per episode, the number of arousals per episode, the ratio of the duration of the respiratory event to the duration of the subsequent between event period, and sleep stage were significantly, if weakly predictive of the % change in HR from the late event phase to between the respiratory events ( Table 3). The model predicted 44% of the % change in HR from the late event phase to between the respiratory events (P < 0.01). This suggests that the more repetitive events compared with isolated events, the more episodes, the more events and arousals per episode a child has, the higher the surge in HR. In contrast, there is a negative relationship between the surge in HR and sleep stage, suggesting that the HR surge is highest during N1 and decreases during N2, N3, and REM. There is also a weak negative relationship between the surge in HR and the ratio of the duration of an event to the duration of the between event period, suggesting that the closer together the events become the % change in HR is not as great.Further analyses separating the repetitive respiratory event episodes into the sleep stage in which they occurred demonstrated that when the episodes occurred during N1 sleep, the predictive variables remained the same as for total sleep. When the episodes occurred during N2 or REM sleep, only the number of arousals in the episode predicted the change in HR (r 2 = 0.3, P < 0.01; REM: r 2 = 0.5, P < 0.001). None of the variables ...

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Hypoxemia alone does not explain blood pressure elevations after obstructive apneas

Cited by 203 publications

References 0 publications

Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

Medicina do sono

Augmented cardiovascular responses to episodes of repetitive compared with isolated respiratory events in preschool children with sleep-disordered breathing

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